Brian F. Mandell, MD, PhD

Primary hypothyroidism is common. Most patients acquire it when the thyroid gland is damaged by autoimmune inflammation. It is readily and reliably treated with the orally administered synthetic hormone levothyroxine, or less reliably with thyroid gland extracts. Absorption of either medication is significantly influenced by food, so patients need to pay attention to the timing of ingestion. But occasional blood testing can be used to easily monitor the sufficiency of replacement therapy.

The predominant active thyroid hormone is triiodothyronine (T₃), most of which is converted from thyroxine (T₄) by deiodination outside of the thyroid gland. Circulating thyroid-binding globulins tie up significant amounts of these hormones in the blood, and this protein binding is affected by a number of factors. Free T₃ and T₄—not bound—are the substances that exert physiologic effects on target organs and also give feedback information to the pituitary gland which, completing the loop, releases thyroid-stimulating hormone (TSH) and ultimately controls the healthy thyroid gland’s production and release of its hormones. Hence, the total circulating thyroid hormone levels are not as biologically relevant as the free T₃ and T₄ levels. Even in the absence of a functioning thyroid gland, the TSH level reliably reflects the bioactivity of circulating thyroid hormones so long as the pituitary gland is functioning normally.

Routine tracking of the biologic effects of thyroid hormone, such as the metabolic rate, is unreasonable, and other biologic effects such as the cholesterol level are influenced by so many factors in addition to T₃ as to be unreliable indicators of thyroid hormone levels. Assuming the patient’s hypothalamic-pituitary axis is normal, the most reasonable and reliable way to track the biologic effect of thyroid hormone is to follow the TSH level. Although the exact relationship between free thyroid hormone and TSH levels is slightly different between patients with normal thyroid glands and those with damaged glands receiving replacement therapy, TSH measurement is an excellent indicator of the level that the brain wants thyroid function to be. Other than in specific nonhomeostatic circumstances, the pituitary gland is usually a superb thermostat for thyroid hormone activity.

In this issue of the Journal, Dr. Christian Nasr discusses the rationale for routinely using TSH measurement alone to direct exogenous thyroid replacement, explaining why it is cost-effective and clinically appropriate.

While following T₃ and T₄ may occasionally be useful in a few patients, the wealth of clinical data does not support this practice. As a routine practice it is certainly financially wasteful, and may lead to inappropriate clinical decisions.

Why, then, do some physicians persist in regularly following T₃ and T₄ levels in addition to TSH? There is no single answer. Although some patients may feel “better” if they take a little more rather than a little less levothyroxine, whether this benefit outweighs the metabolic price in the long run is not at all clear. Plus, in the published experience with treating subclinical hypothyroidism,¹ patients did not generally feel better or experience desired weight loss when they received slightly more exogenous thyroid hormone. Somewhat analogously, if the TSH level is already normal, increasing thyroid replacement to attain a free T₃ or T₄ level in the high-normal range is unlikely to improve clinical outcomes in a meaningful way and may well be detrimental in the long term.

Despite a lot of chatter on Internet blogs regarding the multiple benefits of selective T₃ replacement and higher T₃ levels, akin to testosterone supplementation above what the (normal functioning) hypothalamic-pituitary axis has determined to be biologically appropriate, there is limited clinical evidence to support this practice. When replacing the output of a diseased or absent thyroid gland, it is reasonable clinical practice to trust the pituitary readings of the thyroid thermostat.

Primary hypothyroidism is common. Most patients acquire it when the thyroid gland is damaged by autoimmune inflammation. It is readily and reliably treated with the orally administered synthetic hormone levothyroxine, or less reliably with thyroid gland extracts. Absorption of either medication is significantly influenced by food, so patients need to pay attention to the timing of ingestion. But occasional blood testing can be used to easily monitor the sufficiency of replacement therapy.

The predominant active thyroid hormone is triiodothyronine (T₃), most of which is converted from thyroxine (T₄) by deiodination outside of the thyroid gland. Circulating thyroid-binding globulins tie up significant amounts of these hormones in the blood, and this protein binding is affected by a number of factors. Free T₃ and T₄—not bound—are the substances that exert physiologic effects on target organs and also give feedback information to the pituitary gland which, completing the loop, releases thyroid-stimulating hormone (TSH) and ultimately controls the healthy thyroid gland’s production and release of its hormones. Hence, the total circulating thyroid hormone levels are not as biologically relevant as the free T₃ and T₄ levels. Even in the absence of a functioning thyroid gland, the TSH level reliably reflects the bioactivity of circulating thyroid hormones so long as the pituitary gland is functioning normally.

Routine tracking of the biologic effects of thyroid hormone, such as the metabolic rate, is unreasonable, and other biologic effects such as the cholesterol level are influenced by so many factors in addition to T₃ as to be unreliable indicators of thyroid hormone levels. Assuming the patient’s hypothalamic-pituitary axis is normal, the most reasonable and reliable way to track the biologic effect of thyroid hormone is to follow the TSH level. Although the exact relationship between free thyroid hormone and TSH levels is slightly different between patients with normal thyroid glands and those with damaged glands receiving replacement therapy, TSH measurement is an excellent indicator of the level that the brain wants thyroid function to be. Other than in specific nonhomeostatic circumstances, the pituitary gland is usually a superb thermostat for thyroid hormone activity.

In this issue of the Journal, Dr. Christian Nasr discusses the rationale for routinely using TSH measurement alone to direct exogenous thyroid replacement, explaining why it is cost-effective and clinically appropriate.

While following T₃ and T₄ may occasionally be useful in a few patients, the wealth of clinical data does not support this practice. As a routine practice it is certainly financially wasteful, and may lead to inappropriate clinical decisions.

Why, then, do some physicians persist in regularly following T₃ and T₄ levels in addition to TSH? There is no single answer. Although some patients may feel “better” if they take a little more rather than a little less levothyroxine, whether this benefit outweighs the metabolic price in the long run is not at all clear. Plus, in the published experience with treating subclinical hypothyroidism,¹ patients did not generally feel better or experience desired weight loss when they received slightly more exogenous thyroid hormone. Somewhat analogously, if the TSH level is already normal, increasing thyroid replacement to attain a free T₃ or T₄ level in the high-normal range is unlikely to improve clinical outcomes in a meaningful way and may well be detrimental in the long term.

Despite a lot of chatter on Internet blogs regarding the multiple benefits of selective T₃ replacement and higher T₃ levels, akin to testosterone supplementation above what the (normal functioning) hypothalamic-pituitary axis has determined to be biologically appropriate, there is limited clinical evidence to support this practice. When replacing the output of a diseased or absent thyroid gland, it is reasonable clinical practice to trust the pituitary readings of the thyroid thermostat.

Primary hypothyroidism is common. Most patients acquire it when the thyroid gland is damaged by autoimmune inflammation. It is readily and reliably treated with the orally administered synthetic hormone levothyroxine, or less reliably with thyroid gland extracts. Absorption of either medication is significantly influenced by food, so patients need to pay attention to the timing of ingestion. But occasional blood testing can be used to easily monitor the sufficiency of replacement therapy.

The predominant active thyroid hormone is triiodothyronine (T₃), most of which is converted from thyroxine (T₄) by deiodination outside of the thyroid gland. Circulating thyroid-binding globulins tie up significant amounts of these hormones in the blood, and this protein binding is affected by a number of factors. Free T₃ and T₄—not bound—are the substances that exert physiologic effects on target organs and also give feedback information to the pituitary gland which, completing the loop, releases thyroid-stimulating hormone (TSH) and ultimately controls the healthy thyroid gland’s production and release of its hormones. Hence, the total circulating thyroid hormone levels are not as biologically relevant as the free T₃ and T₄ levels. Even in the absence of a functioning thyroid gland, the TSH level reliably reflects the bioactivity of circulating thyroid hormones so long as the pituitary gland is functioning normally.

Routine tracking of the biologic effects of thyroid hormone, such as the metabolic rate, is unreasonable, and other biologic effects such as the cholesterol level are influenced by so many factors in addition to T₃ as to be unreliable indicators of thyroid hormone levels. Assuming the patient’s hypothalamic-pituitary axis is normal, the most reasonable and reliable way to track the biologic effect of thyroid hormone is to follow the TSH level. Although the exact relationship between free thyroid hormone and TSH levels is slightly different between patients with normal thyroid glands and those with damaged glands receiving replacement therapy, TSH measurement is an excellent indicator of the level that the brain wants thyroid function to be. Other than in specific nonhomeostatic circumstances, the pituitary gland is usually a superb thermostat for thyroid hormone activity.

In this issue of the Journal, Dr. Christian Nasr discusses the rationale for routinely using TSH measurement alone to direct exogenous thyroid replacement, explaining why it is cost-effective and clinically appropriate.

While following T₃ and T₄ may occasionally be useful in a few patients, the wealth of clinical data does not support this practice. As a routine practice it is certainly financially wasteful, and may lead to inappropriate clinical decisions.

Why, then, do some physicians persist in regularly following T₃ and T₄ levels in addition to TSH? There is no single answer. Although some patients may feel “better” if they take a little more rather than a little less levothyroxine, whether this benefit outweighs the metabolic price in the long run is not at all clear. Plus, in the published experience with treating subclinical hypothyroidism,¹ patients did not generally feel better or experience desired weight loss when they received slightly more exogenous thyroid hormone. Somewhat analogously, if the TSH level is already normal, increasing thyroid replacement to attain a free T₃ or T₄ level in the high-normal range is unlikely to improve clinical outcomes in a meaningful way and may well be detrimental in the long term.

Despite a lot of chatter on Internet blogs regarding the multiple benefits of selective T₃ replacement and higher T₃ levels, akin to testosterone supplementation above what the (normal functioning) hypothalamic-pituitary axis has determined to be biologically appropriate, there is limited clinical evidence to support this practice. When replacing the output of a diseased or absent thyroid gland, it is reasonable clinical practice to trust the pituitary readings of the thyroid thermostat.

McNamara and Ng, in this issue of the Journal, discuss the psychosocial and clinical aspects of caring for people who are lesbian, gay, bisexual, or transgender (LGBT), a community that numbers more than 9 million in the United States. Choices for health maintenance and screening are influenced by the patient’s age, sexual practices, comorbidities, and in some transgender patients by current and previous therapeutic hormone manipulations. Although these medical decisions must be personalized, many are informed by existing guidelines for the general population and thus do not represent a dramatic departure from decision-making in other patients.

More difficult is acquiring the requisite understanding and appreciation of the special challenges each LGBT patient brings to the office visit. We need to understand these challenges to provide medically appropriate, compassionate, patient-centered care.

McNamara and Ng suggest simple acts of kindness and consideration to increase the comfort of this group of patients who historically, for a myriad of complex reasons, have not been uniformly made to feel comfortable receiving routine care in our medical system. A tectonic shift has taken place in the way society at large perceives and interacts with members of the LGBT community. Large pockets of intolerance and lack of understanding certainly still exist. But I want to believe that as a medical community, we have changed dramatically over the past several decades.

Early in my medical career, as the AIDS epidemic expanded from unexplained Pneumocystis carinii (now jirovecii) and fungal infections and virulent Kaposi sarcoma to include Guillain-Barré syndrome, central nervous system tumors and infections, and so much more, I watched the gay community rally around specific doctors and medical centers—and avoid others. It was more than just the perception that some hospitals were “gay-friendly.” Care was more compassionate, supportive, and thorough at some hospitals than others. I well recall having difficulty finding a neurosurgeon willing to biopsy a brain mass in one of my patients with AIDS, and finding an orthopedic surgeon willing to manage an infected hip prosthesis in another one. Fast forward 3 decades, and now in a different hospital I am managing gout in a patient who is infected with HIV, is in apparent remission without detectable virus on highly active antiretroviral therapy, and recently received a heart transplant.

As controversies continue to swirl and external acts of discrimination continue to impact the LGBT community on many fronts—bathroom laws, spousal rights, child adoption, gay political leaders, xenophobia, and even hate crimes—it is encouraging to read a matter-of-fact, practical approach to “best practices” in LGBT care. No hype. No judgment. Just compassionate, appropriate medical care.

The journey isn’t over, but there has been progress.

McNamara and Ng, in this issue of the Journal, discuss the psychosocial and clinical aspects of caring for people who are lesbian, gay, bisexual, or transgender (LGBT), a community that numbers more than 9 million in the United States. Choices for health maintenance and screening are influenced by the patient’s age, sexual practices, comorbidities, and in some transgender patients by current and previous therapeutic hormone manipulations. Although these medical decisions must be personalized, many are informed by existing guidelines for the general population and thus do not represent a dramatic departure from decision-making in other patients.

More difficult is acquiring the requisite understanding and appreciation of the special challenges each LGBT patient brings to the office visit. We need to understand these challenges to provide medically appropriate, compassionate, patient-centered care.

McNamara and Ng suggest simple acts of kindness and consideration to increase the comfort of this group of patients who historically, for a myriad of complex reasons, have not been uniformly made to feel comfortable receiving routine care in our medical system. A tectonic shift has taken place in the way society at large perceives and interacts with members of the LGBT community. Large pockets of intolerance and lack of understanding certainly still exist. But I want to believe that as a medical community, we have changed dramatically over the past several decades.

Early in my medical career, as the AIDS epidemic expanded from unexplained Pneumocystis carinii (now jirovecii) and fungal infections and virulent Kaposi sarcoma to include Guillain-Barré syndrome, central nervous system tumors and infections, and so much more, I watched the gay community rally around specific doctors and medical centers—and avoid others. It was more than just the perception that some hospitals were “gay-friendly.” Care was more compassionate, supportive, and thorough at some hospitals than others. I well recall having difficulty finding a neurosurgeon willing to biopsy a brain mass in one of my patients with AIDS, and finding an orthopedic surgeon willing to manage an infected hip prosthesis in another one. Fast forward 3 decades, and now in a different hospital I am managing gout in a patient who is infected with HIV, is in apparent remission without detectable virus on highly active antiretroviral therapy, and recently received a heart transplant.

As controversies continue to swirl and external acts of discrimination continue to impact the LGBT community on many fronts—bathroom laws, spousal rights, child adoption, gay political leaders, xenophobia, and even hate crimes—it is encouraging to read a matter-of-fact, practical approach to “best practices” in LGBT care. No hype. No judgment. Just compassionate, appropriate medical care.

The journey isn’t over, but there has been progress.

McNamara and Ng, in this issue of the Journal, discuss the psychosocial and clinical aspects of caring for people who are lesbian, gay, bisexual, or transgender (LGBT), a community that numbers more than 9 million in the United States. Choices for health maintenance and screening are influenced by the patient’s age, sexual practices, comorbidities, and in some transgender patients by current and previous therapeutic hormone manipulations. Although these medical decisions must be personalized, many are informed by existing guidelines for the general population and thus do not represent a dramatic departure from decision-making in other patients.

More difficult is acquiring the requisite understanding and appreciation of the special challenges each LGBT patient brings to the office visit. We need to understand these challenges to provide medically appropriate, compassionate, patient-centered care.

McNamara and Ng suggest simple acts of kindness and consideration to increase the comfort of this group of patients who historically, for a myriad of complex reasons, have not been uniformly made to feel comfortable receiving routine care in our medical system. A tectonic shift has taken place in the way society at large perceives and interacts with members of the LGBT community. Large pockets of intolerance and lack of understanding certainly still exist. But I want to believe that as a medical community, we have changed dramatically over the past several decades.

Early in my medical career, as the AIDS epidemic expanded from unexplained Pneumocystis carinii (now jirovecii) and fungal infections and virulent Kaposi sarcoma to include Guillain-Barré syndrome, central nervous system tumors and infections, and so much more, I watched the gay community rally around specific doctors and medical centers—and avoid others. It was more than just the perception that some hospitals were “gay-friendly.” Care was more compassionate, supportive, and thorough at some hospitals than others. I well recall having difficulty finding a neurosurgeon willing to biopsy a brain mass in one of my patients with AIDS, and finding an orthopedic surgeon willing to manage an infected hip prosthesis in another one. Fast forward 3 decades, and now in a different hospital I am managing gout in a patient who is infected with HIV, is in apparent remission without detectable virus on highly active antiretroviral therapy, and recently received a heart transplant.

As controversies continue to swirl and external acts of discrimination continue to impact the LGBT community on many fronts—bathroom laws, spousal rights, child adoption, gay political leaders, xenophobia, and even hate crimes—it is encouraging to read a matter-of-fact, practical approach to “best practices” in LGBT care. No hype. No judgment. Just compassionate, appropriate medical care.

The journey isn’t over, but there has been progress.

In this issue of the Journal, Dr. Marissa Galicia-Castillo discusses the use of opioids in older patients with persistent (formerly known as chronic) pain. Even though she devotes one and a half pages to the side effects of chronic opioid therapy, I am sure that in the current environment many readers will perceive her as expressing a surprisingly supportive tone regarding the use of these medications. The times have changed, and the difficulties and complexities of trying to help patients with ongoing pain have increased.

In the mid-1990s, the American Pain Society aggressively pushed the concept of pain as the fifth vital sign.¹ Their stated goals included raising awareness that patients with pain were undertreated, in large part because in the Society’s opinion pain was not regularly assessed at physician office visits or even in the hospital after surgery. Half a decade later the Joint Commission and others hopped on this train, emphasizing that pain needs to be regularly assessed in all patients, that pain is a subjective measure, unlike the heart rate or blood pressure, and that physicians must accept and respect patient self-reporting of pain. Concurrent with these efforts was the enhanced promotion of pain medications—new highly touted and frequently prescribed narcotics as well as nonnarcotic medications re-marketed as analgesics. Opportunistically, or perhaps wielding inappropriate and sketchy influence, some drug manufacturers in the early 2000s funded publications and physician presentations to encourage the expanded use of opioids and other medications for pain control. In a recent CNN report on the opioid epidemic, it was noted that the Joint Commission published a book in 2000 for purchase by doctors as part of required continuing education seminars, and that the book cited studies claiming “there is no evidence that addiction is a significant issue when persons are given opioids for pain control.”² According to the CNN report, the book was sponsored by a manufacturer of narcotic analgesics.² Lack of evidence is not evidence supporting a lack of known concern.

Step forward in time, and pain control has become a measure of patient satisfaction, and thus potentially another physician and institutional rating score that can be linked to reimbursement. This despite reports suggesting that incorporation of this required pain scale did not actually improve the quality of pain management.³ I suspect that most of my peers function in the outpatient clinic as I do, without much interest in what was recorded on the intake pain scale, since I will be taking a more focused and detailed history from the patient if pain is any part of the reason for visiting with me. The goal of alleviating a patient’s pain, whenever reasonable, must always be on our agenda. Yet, while we need to respond to scores on a somewhat silly screening pain scale, the hurdles to prescribing analgesics are getting higher.

The latest data on opioid-related deaths are sobering and scary. Organized medicine must absolutely push to close the pain-pill mills, but is the link really so strong between thoughtful prescribing of short- or even long-term opioids and the escalating “epidemic” of opioid complications that we should not prescribe these drugs? Does the fact that we don’t have good data demonstrating long-term efficacy mean that these drugs are not effective in appropriately selected patients? Is it warranted to require regular database reviews of all patients who are prescribed these medications? Is it warranted, as one patient said to me, that she be treated like a potential criminal begging for drugs when her prescriptions are up, and that she be “looked at funny” by the pharmacist when she fills them?

An increasingly discussed concept is that of central generalization of pain, and patients who have this may be opioid-resistant and, perhaps, prone to developing opioid hyperalgesia. It has been studied in patients with fibromyalgia and is now felt by some to include patients with osteoarthritis and other initially localized painful conditions. Whether or not this concept ultimately turns out to be correct, it adds another dimension to our assessment of patients with pain.

The time has come to move past using a one-size-fits-all fifth vital sign (“How would you rate your pain on a scale of 1 to 10?”) and reflexively prescribing an opioid when pain is characterized as severe. But, if the patient truly needs the drug, we also need to move past not writing that prescription because of headlines and administrative hurdles. This is a much more complex story.

In this issue of the Journal, Dr. Marissa Galicia-Castillo discusses the use of opioids in older patients with persistent (formerly known as chronic) pain. Even though she devotes one and a half pages to the side effects of chronic opioid therapy, I am sure that in the current environment many readers will perceive her as expressing a surprisingly supportive tone regarding the use of these medications. The times have changed, and the difficulties and complexities of trying to help patients with ongoing pain have increased.

In the mid-1990s, the American Pain Society aggressively pushed the concept of pain as the fifth vital sign.¹ Their stated goals included raising awareness that patients with pain were undertreated, in large part because in the Society’s opinion pain was not regularly assessed at physician office visits or even in the hospital after surgery. Half a decade later the Joint Commission and others hopped on this train, emphasizing that pain needs to be regularly assessed in all patients, that pain is a subjective measure, unlike the heart rate or blood pressure, and that physicians must accept and respect patient self-reporting of pain. Concurrent with these efforts was the enhanced promotion of pain medications—new highly touted and frequently prescribed narcotics as well as nonnarcotic medications re-marketed as analgesics. Opportunistically, or perhaps wielding inappropriate and sketchy influence, some drug manufacturers in the early 2000s funded publications and physician presentations to encourage the expanded use of opioids and other medications for pain control. In a recent CNN report on the opioid epidemic, it was noted that the Joint Commission published a book in 2000 for purchase by doctors as part of required continuing education seminars, and that the book cited studies claiming “there is no evidence that addiction is a significant issue when persons are given opioids for pain control.”² According to the CNN report, the book was sponsored by a manufacturer of narcotic analgesics.² Lack of evidence is not evidence supporting a lack of known concern.

Step forward in time, and pain control has become a measure of patient satisfaction, and thus potentially another physician and institutional rating score that can be linked to reimbursement. This despite reports suggesting that incorporation of this required pain scale did not actually improve the quality of pain management.³ I suspect that most of my peers function in the outpatient clinic as I do, without much interest in what was recorded on the intake pain scale, since I will be taking a more focused and detailed history from the patient if pain is any part of the reason for visiting with me. The goal of alleviating a patient’s pain, whenever reasonable, must always be on our agenda. Yet, while we need to respond to scores on a somewhat silly screening pain scale, the hurdles to prescribing analgesics are getting higher.

The latest data on opioid-related deaths are sobering and scary. Organized medicine must absolutely push to close the pain-pill mills, but is the link really so strong between thoughtful prescribing of short- or even long-term opioids and the escalating “epidemic” of opioid complications that we should not prescribe these drugs? Does the fact that we don’t have good data demonstrating long-term efficacy mean that these drugs are not effective in appropriately selected patients? Is it warranted to require regular database reviews of all patients who are prescribed these medications? Is it warranted, as one patient said to me, that she be treated like a potential criminal begging for drugs when her prescriptions are up, and that she be “looked at funny” by the pharmacist when she fills them?

An increasingly discussed concept is that of central generalization of pain, and patients who have this may be opioid-resistant and, perhaps, prone to developing opioid hyperalgesia. It has been studied in patients with fibromyalgia and is now felt by some to include patients with osteoarthritis and other initially localized painful conditions. Whether or not this concept ultimately turns out to be correct, it adds another dimension to our assessment of patients with pain.

The time has come to move past using a one-size-fits-all fifth vital sign (“How would you rate your pain on a scale of 1 to 10?”) and reflexively prescribing an opioid when pain is characterized as severe. But, if the patient truly needs the drug, we also need to move past not writing that prescription because of headlines and administrative hurdles. This is a much more complex story.

In this issue of the Journal, Dr. Marissa Galicia-Castillo discusses the use of opioids in older patients with persistent (formerly known as chronic) pain. Even though she devotes one and a half pages to the side effects of chronic opioid therapy, I am sure that in the current environment many readers will perceive her as expressing a surprisingly supportive tone regarding the use of these medications. The times have changed, and the difficulties and complexities of trying to help patients with ongoing pain have increased.

In the mid-1990s, the American Pain Society aggressively pushed the concept of pain as the fifth vital sign.¹ Their stated goals included raising awareness that patients with pain were undertreated, in large part because in the Society’s opinion pain was not regularly assessed at physician office visits or even in the hospital after surgery. Half a decade later the Joint Commission and others hopped on this train, emphasizing that pain needs to be regularly assessed in all patients, that pain is a subjective measure, unlike the heart rate or blood pressure, and that physicians must accept and respect patient self-reporting of pain. Concurrent with these efforts was the enhanced promotion of pain medications—new highly touted and frequently prescribed narcotics as well as nonnarcotic medications re-marketed as analgesics. Opportunistically, or perhaps wielding inappropriate and sketchy influence, some drug manufacturers in the early 2000s funded publications and physician presentations to encourage the expanded use of opioids and other medications for pain control. In a recent CNN report on the opioid epidemic, it was noted that the Joint Commission published a book in 2000 for purchase by doctors as part of required continuing education seminars, and that the book cited studies claiming “there is no evidence that addiction is a significant issue when persons are given opioids for pain control.”² According to the CNN report, the book was sponsored by a manufacturer of narcotic analgesics.² Lack of evidence is not evidence supporting a lack of known concern.

Step forward in time, and pain control has become a measure of patient satisfaction, and thus potentially another physician and institutional rating score that can be linked to reimbursement. This despite reports suggesting that incorporation of this required pain scale did not actually improve the quality of pain management.³ I suspect that most of my peers function in the outpatient clinic as I do, without much interest in what was recorded on the intake pain scale, since I will be taking a more focused and detailed history from the patient if pain is any part of the reason for visiting with me. The goal of alleviating a patient’s pain, whenever reasonable, must always be on our agenda. Yet, while we need to respond to scores on a somewhat silly screening pain scale, the hurdles to prescribing analgesics are getting higher.

The latest data on opioid-related deaths are sobering and scary. Organized medicine must absolutely push to close the pain-pill mills, but is the link really so strong between thoughtful prescribing of short- or even long-term opioids and the escalating “epidemic” of opioid complications that we should not prescribe these drugs? Does the fact that we don’t have good data demonstrating long-term efficacy mean that these drugs are not effective in appropriately selected patients? Is it warranted to require regular database reviews of all patients who are prescribed these medications? Is it warranted, as one patient said to me, that she be treated like a potential criminal begging for drugs when her prescriptions are up, and that she be “looked at funny” by the pharmacist when she fills them?

An increasingly discussed concept is that of central generalization of pain, and patients who have this may be opioid-resistant and, perhaps, prone to developing opioid hyperalgesia. It has been studied in patients with fibromyalgia and is now felt by some to include patients with osteoarthritis and other initially localized painful conditions. Whether or not this concept ultimately turns out to be correct, it adds another dimension to our assessment of patients with pain.

The time has come to move past using a one-size-fits-all fifth vital sign (“How would you rate your pain on a scale of 1 to 10?”) and reflexively prescribing an opioid when pain is characterized as severe. But, if the patient truly needs the drug, we also need to move past not writing that prescription because of headlines and administrative hurdles. This is a much more complex story.

Quinn and Fang, in this issue of the Journal discuss efforts to predict bleeding complications associated with anticoagulant therapy in elderly patients. They note, as others have suggested, that we may fear the risk of severe anticoagulant-associated bleeding more than is warranted based on the data. The level of that fear and the risk of bleeding depend on the specific need for anticoagulant therapy in a given patient and on the risk of serious adverse outcomes from thrombosis that the anticoagulation is supposed to prevent. All prediction models are based on an “average” patient with certain characteristics. But of course none of our patients are average.

The studies Quinn and Fang discuss focus on vitamin K antagonist therapy. There is probably not enough practice-based or trial-based evidence yet to evaluate the risks associated with the new generation of anticoagulants.

All prediction models have limitations. The recent discussion on establishing a risk-based strategy to guide institution of lipid-lowering therapy highlights the challenges inherent in trying to base therapeutic decisions on predictive models. But however imperfect, models are still widely used to predict fracture risk in patients being considered for bone antiresorptive therapy and to predict the need for anticoagulation therapy or further diagnostic testing in patients with potential deep vein thrombosis or atrial fibrillation.

The decision to start anticoagulation in an elderly patient is often informed by the possibility of an easily recognized and feared risk factor for bleeding complications—falling. Falls are certainly important and are a major contributor to subdural hematoma and complicated hip fracture. But there are more common causes of severe bleeding complications that are less easily predicted by functional assessment of the patient. Nonetheless, fall risk can be lessened by prescribing exercise programs such as tai chi to improve balance, limiting the use of drugs associated with falls in the elderly, perhaps correcting hyponatremia, and testing for orthostatic hypotension as part of the physical examination. (Mild compression stockings and medication adjustment may reduce orthostasis.) Some of these interventions are easily accomplished, and probably should be done with all of our elderly and frail patients.

As we build more risk calculators into our electronic medical records, we must continue to consider their limitations as well as their specific utility. To paraphrase Yogi Berra, making predictions is tough, especially about the future.

Quinn and Fang, in this issue of the Journal discuss efforts to predict bleeding complications associated with anticoagulant therapy in elderly patients. They note, as others have suggested, that we may fear the risk of severe anticoagulant-associated bleeding more than is warranted based on the data. The level of that fear and the risk of bleeding depend on the specific need for anticoagulant therapy in a given patient and on the risk of serious adverse outcomes from thrombosis that the anticoagulation is supposed to prevent. All prediction models are based on an “average” patient with certain characteristics. But of course none of our patients are average.

The studies Quinn and Fang discuss focus on vitamin K antagonist therapy. There is probably not enough practice-based or trial-based evidence yet to evaluate the risks associated with the new generation of anticoagulants.

All prediction models have limitations. The recent discussion on establishing a risk-based strategy to guide institution of lipid-lowering therapy highlights the challenges inherent in trying to base therapeutic decisions on predictive models. But however imperfect, models are still widely used to predict fracture risk in patients being considered for bone antiresorptive therapy and to predict the need for anticoagulation therapy or further diagnostic testing in patients with potential deep vein thrombosis or atrial fibrillation.

The decision to start anticoagulation in an elderly patient is often informed by the possibility of an easily recognized and feared risk factor for bleeding complications—falling. Falls are certainly important and are a major contributor to subdural hematoma and complicated hip fracture. But there are more common causes of severe bleeding complications that are less easily predicted by functional assessment of the patient. Nonetheless, fall risk can be lessened by prescribing exercise programs such as tai chi to improve balance, limiting the use of drugs associated with falls in the elderly, perhaps correcting hyponatremia, and testing for orthostatic hypotension as part of the physical examination. (Mild compression stockings and medication adjustment may reduce orthostasis.) Some of these interventions are easily accomplished, and probably should be done with all of our elderly and frail patients.

As we build more risk calculators into our electronic medical records, we must continue to consider their limitations as well as their specific utility. To paraphrase Yogi Berra, making predictions is tough, especially about the future.

Quinn and Fang, in this issue of the Journal discuss efforts to predict bleeding complications associated with anticoagulant therapy in elderly patients. They note, as others have suggested, that we may fear the risk of severe anticoagulant-associated bleeding more than is warranted based on the data. The level of that fear and the risk of bleeding depend on the specific need for anticoagulant therapy in a given patient and on the risk of serious adverse outcomes from thrombosis that the anticoagulation is supposed to prevent. All prediction models are based on an “average” patient with certain characteristics. But of course none of our patients are average.

The studies Quinn and Fang discuss focus on vitamin K antagonist therapy. There is probably not enough practice-based or trial-based evidence yet to evaluate the risks associated with the new generation of anticoagulants.

All prediction models have limitations. The recent discussion on establishing a risk-based strategy to guide institution of lipid-lowering therapy highlights the challenges inherent in trying to base therapeutic decisions on predictive models. But however imperfect, models are still widely used to predict fracture risk in patients being considered for bone antiresorptive therapy and to predict the need for anticoagulation therapy or further diagnostic testing in patients with potential deep vein thrombosis or atrial fibrillation.

The decision to start anticoagulation in an elderly patient is often informed by the possibility of an easily recognized and feared risk factor for bleeding complications—falling. Falls are certainly important and are a major contributor to subdural hematoma and complicated hip fracture. But there are more common causes of severe bleeding complications that are less easily predicted by functional assessment of the patient. Nonetheless, fall risk can be lessened by prescribing exercise programs such as tai chi to improve balance, limiting the use of drugs associated with falls in the elderly, perhaps correcting hyponatremia, and testing for orthostatic hypotension as part of the physical examination. (Mild compression stockings and medication adjustment may reduce orthostasis.) Some of these interventions are easily accomplished, and probably should be done with all of our elderly and frail patients.

As we build more risk calculators into our electronic medical records, we must continue to consider their limitations as well as their specific utility. To paraphrase Yogi Berra, making predictions is tough, especially about the future.

The latest reminders that we live in a medically connected global community are the appearance of the Africa-born Zika virus infection in Brazil and other areas within the Western hemisphere and the subsequent apparent transmission of the disease to female sexual contacts of infected males in the United States. Zika virus’ geographic travels are most certainly of interest; they can be traced from sub-Saharan Africa, where serologically identified outbreaks have continued since 1947, through Asia, Micronesia, Polynesia, and now South and Central America. But what may turn out to be even more interesting than the virus’s travel itinerary is what we may learn about the Zika virus-human host interaction and the subsequent spectrum of clinical disease.

The primary clinical illness following serologically defined infection seems to be relatively uncommon and generally mild: a fairly nondistinctive febrile episode with mild rash, small- and large-joint arthralgias or arthritis, and nonpurulent conjunctivitis. But what has fostered the greatest concern is the epidemiologic association of Zika infection with the neurologic complications of microcephaly and Guillain-Barré syndrome (GBS).

During the 2013–2014 outbreak of Zika infection in French Polynesia, 42 patients with GBS were identified, 100% of whom had serologic evidence suggestive of recent Zika infection, compared with 56% of control patients without GBS.¹ Serologic determination of recent infection can be difficult due to cross-reactivity with other flaviviruses, but it seems that in the Polynesian outbreak the risk of GBS might be much less than 1 in 1,000 patients. This is not unlike the incidence of GBS following influenza, Campylobacter, and cytomegalovirus. One explanation for why GBS may follow certain infections is that the infection can trigger antibodies that cross-react with neuronal membrane components. However, those antiganglioside antibodies were not uniformly present in the Polynesian patients who developed GBS following Zika infection. Thus, this may provide an opportunity to further understand the mechanism by which GBS is associated with some infections, in selected patients.

Patients with post-Zika GBS seem to fare well, with a very good prognosis for complete recovery. That is not the case, however, for infants born with microcephaly, another epidemiologically linked complication of Zika infection. In Brazil, the exact incidence rate remains to be determined, and it is not yet certain whether the rate is higher than in the previous Polynesian epidemic (the number of infections is far greater in Brazil, and thus the accuracy of estimated frequency may also be greater), but there may have been a significantly increased frequency of microcephaly in the Polynesian outbreak as well. Like the related West Nile, Saint Louis encephalitis, and Japanese encephalitis viruses, Zika virus has the ability to directly attack certain neurons, and the Zika genome has been detected in brains of infected babies at autopsy. So this particularly devastating aspect of Zika infection may turn out to be relatively easy to understand—perhaps the portal for viral infection of specific neurons is expressed only at certain times during brain development. I’m sure these investigations are under way at a feverish pitch.

Recognizing that new information is being released virtually daily, Flores et al provide a current overview of our understanding of the virus and some practical advice regarding diagnosis and prevention.

As laboratories gear up to devise rapid and more specific diagnostic tests and develop effective anti-Zika vaccines, we hope to learn more about how a seemingly minimally relevant virus, when introduced into a new environment, can wreak clinical havoc. Possible explanations abound—genetic differences in the population, altered immunologic background of infected patients due to prior infection with related viruses such as dengue, or the direct impact of other coinfections. Or, with careful study, it may be discovered that these neurologic issues have been present elsewhere all along, but not previously linked to the Zika virus.

The latest reminders that we live in a medically connected global community are the appearance of the Africa-born Zika virus infection in Brazil and other areas within the Western hemisphere and the subsequent apparent transmission of the disease to female sexual contacts of infected males in the United States. Zika virus’ geographic travels are most certainly of interest; they can be traced from sub-Saharan Africa, where serologically identified outbreaks have continued since 1947, through Asia, Micronesia, Polynesia, and now South and Central America. But what may turn out to be even more interesting than the virus’s travel itinerary is what we may learn about the Zika virus-human host interaction and the subsequent spectrum of clinical disease.

The primary clinical illness following serologically defined infection seems to be relatively uncommon and generally mild: a fairly nondistinctive febrile episode with mild rash, small- and large-joint arthralgias or arthritis, and nonpurulent conjunctivitis. But what has fostered the greatest concern is the epidemiologic association of Zika infection with the neurologic complications of microcephaly and Guillain-Barré syndrome (GBS).

During the 2013–2014 outbreak of Zika infection in French Polynesia, 42 patients with GBS were identified, 100% of whom had serologic evidence suggestive of recent Zika infection, compared with 56% of control patients without GBS.¹ Serologic determination of recent infection can be difficult due to cross-reactivity with other flaviviruses, but it seems that in the Polynesian outbreak the risk of GBS might be much less than 1 in 1,000 patients. This is not unlike the incidence of GBS following influenza, Campylobacter, and cytomegalovirus. One explanation for why GBS may follow certain infections is that the infection can trigger antibodies that cross-react with neuronal membrane components. However, those antiganglioside antibodies were not uniformly present in the Polynesian patients who developed GBS following Zika infection. Thus, this may provide an opportunity to further understand the mechanism by which GBS is associated with some infections, in selected patients.

Patients with post-Zika GBS seem to fare well, with a very good prognosis for complete recovery. That is not the case, however, for infants born with microcephaly, another epidemiologically linked complication of Zika infection. In Brazil, the exact incidence rate remains to be determined, and it is not yet certain whether the rate is higher than in the previous Polynesian epidemic (the number of infections is far greater in Brazil, and thus the accuracy of estimated frequency may also be greater), but there may have been a significantly increased frequency of microcephaly in the Polynesian outbreak as well. Like the related West Nile, Saint Louis encephalitis, and Japanese encephalitis viruses, Zika virus has the ability to directly attack certain neurons, and the Zika genome has been detected in brains of infected babies at autopsy. So this particularly devastating aspect of Zika infection may turn out to be relatively easy to understand—perhaps the portal for viral infection of specific neurons is expressed only at certain times during brain development. I’m sure these investigations are under way at a feverish pitch.

Recognizing that new information is being released virtually daily, Flores et al provide a current overview of our understanding of the virus and some practical advice regarding diagnosis and prevention.

As laboratories gear up to devise rapid and more specific diagnostic tests and develop effective anti-Zika vaccines, we hope to learn more about how a seemingly minimally relevant virus, when introduced into a new environment, can wreak clinical havoc. Possible explanations abound—genetic differences in the population, altered immunologic background of infected patients due to prior infection with related viruses such as dengue, or the direct impact of other coinfections. Or, with careful study, it may be discovered that these neurologic issues have been present elsewhere all along, but not previously linked to the Zika virus.

The latest reminders that we live in a medically connected global community are the appearance of the Africa-born Zika virus infection in Brazil and other areas within the Western hemisphere and the subsequent apparent transmission of the disease to female sexual contacts of infected males in the United States. Zika virus’ geographic travels are most certainly of interest; they can be traced from sub-Saharan Africa, where serologically identified outbreaks have continued since 1947, through Asia, Micronesia, Polynesia, and now South and Central America. But what may turn out to be even more interesting than the virus’s travel itinerary is what we may learn about the Zika virus-human host interaction and the subsequent spectrum of clinical disease.

The primary clinical illness following serologically defined infection seems to be relatively uncommon and generally mild: a fairly nondistinctive febrile episode with mild rash, small- and large-joint arthralgias or arthritis, and nonpurulent conjunctivitis. But what has fostered the greatest concern is the epidemiologic association of Zika infection with the neurologic complications of microcephaly and Guillain-Barré syndrome (GBS).

During the 2013–2014 outbreak of Zika infection in French Polynesia, 42 patients with GBS were identified, 100% of whom had serologic evidence suggestive of recent Zika infection, compared with 56% of control patients without GBS.¹ Serologic determination of recent infection can be difficult due to cross-reactivity with other flaviviruses, but it seems that in the Polynesian outbreak the risk of GBS might be much less than 1 in 1,000 patients. This is not unlike the incidence of GBS following influenza, Campylobacter, and cytomegalovirus. One explanation for why GBS may follow certain infections is that the infection can trigger antibodies that cross-react with neuronal membrane components. However, those antiganglioside antibodies were not uniformly present in the Polynesian patients who developed GBS following Zika infection. Thus, this may provide an opportunity to further understand the mechanism by which GBS is associated with some infections, in selected patients.

Patients with post-Zika GBS seem to fare well, with a very good prognosis for complete recovery. That is not the case, however, for infants born with microcephaly, another epidemiologically linked complication of Zika infection. In Brazil, the exact incidence rate remains to be determined, and it is not yet certain whether the rate is higher than in the previous Polynesian epidemic (the number of infections is far greater in Brazil, and thus the accuracy of estimated frequency may also be greater), but there may have been a significantly increased frequency of microcephaly in the Polynesian outbreak as well. Like the related West Nile, Saint Louis encephalitis, and Japanese encephalitis viruses, Zika virus has the ability to directly attack certain neurons, and the Zika genome has been detected in brains of infected babies at autopsy. So this particularly devastating aspect of Zika infection may turn out to be relatively easy to understand—perhaps the portal for viral infection of specific neurons is expressed only at certain times during brain development. I’m sure these investigations are under way at a feverish pitch.

Recognizing that new information is being released virtually daily, Flores et al provide a current overview of our understanding of the virus and some practical advice regarding diagnosis and prevention.

As laboratories gear up to devise rapid and more specific diagnostic tests and develop effective anti-Zika vaccines, we hope to learn more about how a seemingly minimally relevant virus, when introduced into a new environment, can wreak clinical havoc. Possible explanations abound—genetic differences in the population, altered immunologic background of infected patients due to prior infection with related viruses such as dengue, or the direct impact of other coinfections. Or, with careful study, it may be discovered that these neurologic issues have been present elsewhere all along, but not previously linked to the Zika virus.

“I am forever humbled.” So said a heart failure specialist on rounds when I was a resident in the intensive care unit several decades ago. He was talking about the perpetual mismatch between a physician’s level of knowledge and the unpredictability inherent in the management and outcome of critically ill patients. His words ring true for me nearly every day. We should never think we are so smart that we are truly in control of our patients’ outcomes or that we don’t make mistakes—but we also cannot become so paralyzed by the awareness of our limitations that we don’t make decisions.

I have spoken those same powerful words many times on teaching rounds. I also frequently push them to the back of my mind. As a consultant at a major medical center, I am supposed to know. It is a fine line we walk.

I know I am not alone in harboring these self-doubts. Ready access to online information does little to assuage the concern that we can never know enough. Have I ordered enough diagnostic tests to be sure? Have I ordered too many tests and thus will be penalized for providing cost-ineffective care? Should we follow generic guidelines, or deviate from the guidelines based on our clinical instincts, our own interpretation of the literature, and the patient’s unique circumstances and desires?

And then what happens when we make wrong decisions, or even the right decisions that result in a poor patient outcome, which of course is at some point inevitable? We are told to be open about errors, to be honest and transparent about our limitations, to throw down our elaborate emotional and intellectual defensive shields and expose our vulnerability.

But what do we experience emotionally when we are named in a malpractice suit? We may have done all that we thought we could do: we responsibly explored the diagnostic and therapeutic options, provided empathetic care, and listened to the voice of the patient. Yet an adverse outcome still occurred. The practice of medicine is indeed humbling. We feel crushed. We revisit the patient’s care in a vivid perpetual replay loop in our head. Maybe we didn’t evaluate all the options as we should have. If we had been a bit smarter, a bit more efficient, maybe the outcome would have been different.

Then during a deposition, the plaintiff’s counsel points out the temporal and documentary inconsistencies in the electronic medical record: “Doctor, you say you saw the patient at 2:00 pm, but there was no note finalized until 10:00 pm…and why was your documented physical exam exactly the same as the one from the day before and exactly the same as that of the resident who saw the patient that afternoon?” We now feel crushed, totally vulnerable, emotionally trampled, and often isolated and disconnected from our patients and peers. The intellectualized humility becomes transformed into a sense of inadequacy. Why should I keep doing this?

In this issue of the Journal, experienced malpractice attorney Kevin Giordano explores aspects of the malpractice process as they relate to the physicians he defends. He notes how the electronic medical record, a tool ostensibly in place to improve communication and the sharing of medical information between caregivers and patients, can be our worst enemy in a courtroom. He discusses the pressures of our complicated healthcare system that promote documentation errors that he must try to explain away to the jury in our defense, demonstrating that these documentation errors do not necessarily mirror the care and caring of the named physicians. This is critically important information for us to understand and to act on for our personal protection, but it is not his most important message to us.

Mr. Giordano is a sincere, empathetic, and proficient professional. He has spoken for and to many physicians. He has listened to us and observed our behaviors. And as he has defended many of us in a court of law, he has learned to diagnose in his clients the damage that can persist following involvement in a malpractice case and the emotional scars the malpractice experience leaves on physicians. He emphasizes that we must not let the event of a malpractice suit force us to withdraw and strip us of our connection and engagement to patients. If anything, he and Drs. Susan Rehm and Bradford Borden, in an accompanying editorial, urge us to keep in mind that our personal engagement with patients and the mindful practice of medicine is our raison d’être as physicians.

I am continuously humbled by the breadth of the pathology, clinical medicine, and social challenges that I encounter on a daily basis, armed with limited knowledge and experience. It is intellectually rewarding to make an arcane diagnosis or to see an individualized therapy work as I had hoped. But I agree with Mr. Giordano that it is the genuine engagement with patients that provides us with the real joy in the practice of medicine and pushes us to deliver care at a consistently proficient level. We must not forget that, even in the face of significant and emotionally challenging events such as being named in a malpractice suit. It is the nature of our engagement with our patients and our colleagues that make what we do more than a job.

As more physicians in the United States become employed by health systems, I hope that the administrative leaders within these systems truly recognize these issues. As they struggle to balance the provision of safe high-quality care to patients with their increasingly complex financial spreadsheets, I hope that the emotional health of their physician employees is not forgotten. And not just after a malpractice suit.

“I am forever humbled.” So said a heart failure specialist on rounds when I was a resident in the intensive care unit several decades ago. He was talking about the perpetual mismatch between a physician’s level of knowledge and the unpredictability inherent in the management and outcome of critically ill patients. His words ring true for me nearly every day. We should never think we are so smart that we are truly in control of our patients’ outcomes or that we don’t make mistakes—but we also cannot become so paralyzed by the awareness of our limitations that we don’t make decisions.

I have spoken those same powerful words many times on teaching rounds. I also frequently push them to the back of my mind. As a consultant at a major medical center, I am supposed to know. It is a fine line we walk.

I know I am not alone in harboring these self-doubts. Ready access to online information does little to assuage the concern that we can never know enough. Have I ordered enough diagnostic tests to be sure? Have I ordered too many tests and thus will be penalized for providing cost-ineffective care? Should we follow generic guidelines, or deviate from the guidelines based on our clinical instincts, our own interpretation of the literature, and the patient’s unique circumstances and desires?

And then what happens when we make wrong decisions, or even the right decisions that result in a poor patient outcome, which of course is at some point inevitable? We are told to be open about errors, to be honest and transparent about our limitations, to throw down our elaborate emotional and intellectual defensive shields and expose our vulnerability.

But what do we experience emotionally when we are named in a malpractice suit? We may have done all that we thought we could do: we responsibly explored the diagnostic and therapeutic options, provided empathetic care, and listened to the voice of the patient. Yet an adverse outcome still occurred. The practice of medicine is indeed humbling. We feel crushed. We revisit the patient’s care in a vivid perpetual replay loop in our head. Maybe we didn’t evaluate all the options as we should have. If we had been a bit smarter, a bit more efficient, maybe the outcome would have been different.

Then during a deposition, the plaintiff’s counsel points out the temporal and documentary inconsistencies in the electronic medical record: “Doctor, you say you saw the patient at 2:00 pm, but there was no note finalized until 10:00 pm…and why was your documented physical exam exactly the same as the one from the day before and exactly the same as that of the resident who saw the patient that afternoon?” We now feel crushed, totally vulnerable, emotionally trampled, and often isolated and disconnected from our patients and peers. The intellectualized humility becomes transformed into a sense of inadequacy. Why should I keep doing this?

In this issue of the Journal, experienced malpractice attorney Kevin Giordano explores aspects of the malpractice process as they relate to the physicians he defends. He notes how the electronic medical record, a tool ostensibly in place to improve communication and the sharing of medical information between caregivers and patients, can be our worst enemy in a courtroom. He discusses the pressures of our complicated healthcare system that promote documentation errors that he must try to explain away to the jury in our defense, demonstrating that these documentation errors do not necessarily mirror the care and caring of the named physicians. This is critically important information for us to understand and to act on for our personal protection, but it is not his most important message to us.

Mr. Giordano is a sincere, empathetic, and proficient professional. He has spoken for and to many physicians. He has listened to us and observed our behaviors. And as he has defended many of us in a court of law, he has learned to diagnose in his clients the damage that can persist following involvement in a malpractice case and the emotional scars the malpractice experience leaves on physicians. He emphasizes that we must not let the event of a malpractice suit force us to withdraw and strip us of our connection and engagement to patients. If anything, he and Drs. Susan Rehm and Bradford Borden, in an accompanying editorial, urge us to keep in mind that our personal engagement with patients and the mindful practice of medicine is our raison d’être as physicians.

I am continuously humbled by the breadth of the pathology, clinical medicine, and social challenges that I encounter on a daily basis, armed with limited knowledge and experience. It is intellectually rewarding to make an arcane diagnosis or to see an individualized therapy work as I had hoped. But I agree with Mr. Giordano that it is the genuine engagement with patients that provides us with the real joy in the practice of medicine and pushes us to deliver care at a consistently proficient level. We must not forget that, even in the face of significant and emotionally challenging events such as being named in a malpractice suit. It is the nature of our engagement with our patients and our colleagues that make what we do more than a job.

As more physicians in the United States become employed by health systems, I hope that the administrative leaders within these systems truly recognize these issues. As they struggle to balance the provision of safe high-quality care to patients with their increasingly complex financial spreadsheets, I hope that the emotional health of their physician employees is not forgotten. And not just after a malpractice suit.

“I am forever humbled.” So said a heart failure specialist on rounds when I was a resident in the intensive care unit several decades ago. He was talking about the perpetual mismatch between a physician’s level of knowledge and the unpredictability inherent in the management and outcome of critically ill patients. His words ring true for me nearly every day. We should never think we are so smart that we are truly in control of our patients’ outcomes or that we don’t make mistakes—but we also cannot become so paralyzed by the awareness of our limitations that we don’t make decisions.

I have spoken those same powerful words many times on teaching rounds. I also frequently push them to the back of my mind. As a consultant at a major medical center, I am supposed to know. It is a fine line we walk.

I know I am not alone in harboring these self-doubts. Ready access to online information does little to assuage the concern that we can never know enough. Have I ordered enough diagnostic tests to be sure? Have I ordered too many tests and thus will be penalized for providing cost-ineffective care? Should we follow generic guidelines, or deviate from the guidelines based on our clinical instincts, our own interpretation of the literature, and the patient’s unique circumstances and desires?

And then what happens when we make wrong decisions, or even the right decisions that result in a poor patient outcome, which of course is at some point inevitable? We are told to be open about errors, to be honest and transparent about our limitations, to throw down our elaborate emotional and intellectual defensive shields and expose our vulnerability.

But what do we experience emotionally when we are named in a malpractice suit? We may have done all that we thought we could do: we responsibly explored the diagnostic and therapeutic options, provided empathetic care, and listened to the voice of the patient. Yet an adverse outcome still occurred. The practice of medicine is indeed humbling. We feel crushed. We revisit the patient’s care in a vivid perpetual replay loop in our head. Maybe we didn’t evaluate all the options as we should have. If we had been a bit smarter, a bit more efficient, maybe the outcome would have been different.

Then during a deposition, the plaintiff’s counsel points out the temporal and documentary inconsistencies in the electronic medical record: “Doctor, you say you saw the patient at 2:00 pm, but there was no note finalized until 10:00 pm…and why was your documented physical exam exactly the same as the one from the day before and exactly the same as that of the resident who saw the patient that afternoon?” We now feel crushed, totally vulnerable, emotionally trampled, and often isolated and disconnected from our patients and peers. The intellectualized humility becomes transformed into a sense of inadequacy. Why should I keep doing this?

In this issue of the Journal, experienced malpractice attorney Kevin Giordano explores aspects of the malpractice process as they relate to the physicians he defends. He notes how the electronic medical record, a tool ostensibly in place to improve communication and the sharing of medical information between caregivers and patients, can be our worst enemy in a courtroom. He discusses the pressures of our complicated healthcare system that promote documentation errors that he must try to explain away to the jury in our defense, demonstrating that these documentation errors do not necessarily mirror the care and caring of the named physicians. This is critically important information for us to understand and to act on for our personal protection, but it is not his most important message to us.

Mr. Giordano is a sincere, empathetic, and proficient professional. He has spoken for and to many physicians. He has listened to us and observed our behaviors. And as he has defended many of us in a court of law, he has learned to diagnose in his clients the damage that can persist following involvement in a malpractice case and the emotional scars the malpractice experience leaves on physicians. He emphasizes that we must not let the event of a malpractice suit force us to withdraw and strip us of our connection and engagement to patients. If anything, he and Drs. Susan Rehm and Bradford Borden, in an accompanying editorial, urge us to keep in mind that our personal engagement with patients and the mindful practice of medicine is our raison d’être as physicians.

I am continuously humbled by the breadth of the pathology, clinical medicine, and social challenges that I encounter on a daily basis, armed with limited knowledge and experience. It is intellectually rewarding to make an arcane diagnosis or to see an individualized therapy work as I had hoped. But I agree with Mr. Giordano that it is the genuine engagement with patients that provides us with the real joy in the practice of medicine and pushes us to deliver care at a consistently proficient level. We must not forget that, even in the face of significant and emotionally challenging events such as being named in a malpractice suit. It is the nature of our engagement with our patients and our colleagues that make what we do more than a job.

As more physicians in the United States become employed by health systems, I hope that the administrative leaders within these systems truly recognize these issues. As they struggle to balance the provision of safe high-quality care to patients with their increasingly complex financial spreadsheets, I hope that the emotional health of their physician employees is not forgotten. And not just after a malpractice suit.

Judging by the crowd and the difficulty in finding a locker at my gym on January 1, a lot of people are serious about their 2016 New Year’s resolution to exercise and lose weight. But as most of us have experienced personally and professionally, embarking on a well-intended effort to exercise in the hope of losing weight more often results in frustration than a trip to the store to buy smaller-sized clothes.

The frequent answer to the question “What did the doctor say at your visit?” provides a partial explanation of this phenomenon: “Nothing, just that I should exercise and lose weight” is the usual hackneyed response. Nothing—as in nothing unexpected, nothing significant, and nothing specific was said. It is with this lack of specific advice that I feel many of us let our patients down.

We admonish patients to eat fewer calories, avoid the evil carbs, walk 10,000 steps, ride a bike, use the elliptical, or swim three times a week. There is a concrete but broad nature to these suggestions, but there is also a familiarity and a lack of specificity that leaves patients feeling that there is no science behind them. And the truth is that many of us are not comfortable enough with current data from our exercise physiology colleagues to have a detailed discussion with our patients that pairs their specific goals with an exercise regimen and diet most likely to be beneficial. We may fear sounding like the morning talk show doctors, offering sound bites instead of engaging in an evidence-based dialogue with our patients.

Many of our patients cannot afford a personal trainer to guide and cajole them through a successful regimen—assuming that they, or we, can separate myth and fact and choose an appropriate trainer. We should try to be their guide and sounding board as well as coach and cheerleader.

In this issue of the Journal, John and Christopher Higgins present a primer on the background information to use when talking with our patients about starting an exercise program focused on weight loss. They provide useful references that support specific approaches to achieve realistic expectations, and they review and compare various strategies.

I’m sure by March it will again be easier to find a locker at my gym. And I hope by then that my new workout plan will be more scientifically based, as well as a bit more effective. Even data-based hope springs eternal.

Judging by the crowd and the difficulty in finding a locker at my gym on January 1, a lot of people are serious about their 2016 New Year’s resolution to exercise and lose weight. But as most of us have experienced personally and professionally, embarking on a well-intended effort to exercise in the hope of losing weight more often results in frustration than a trip to the store to buy smaller-sized clothes.

The frequent answer to the question “What did the doctor say at your visit?” provides a partial explanation of this phenomenon: “Nothing, just that I should exercise and lose weight” is the usual hackneyed response. Nothing—as in nothing unexpected, nothing significant, and nothing specific was said. It is with this lack of specific advice that I feel many of us let our patients down.

We admonish patients to eat fewer calories, avoid the evil carbs, walk 10,000 steps, ride a bike, use the elliptical, or swim three times a week. There is a concrete but broad nature to these suggestions, but there is also a familiarity and a lack of specificity that leaves patients feeling that there is no science behind them. And the truth is that many of us are not comfortable enough with current data from our exercise physiology colleagues to have a detailed discussion with our patients that pairs their specific goals with an exercise regimen and diet most likely to be beneficial. We may fear sounding like the morning talk show doctors, offering sound bites instead of engaging in an evidence-based dialogue with our patients.

Many of our patients cannot afford a personal trainer to guide and cajole them through a successful regimen—assuming that they, or we, can separate myth and fact and choose an appropriate trainer. We should try to be their guide and sounding board as well as coach and cheerleader.

In this issue of the Journal, John and Christopher Higgins present a primer on the background information to use when talking with our patients about starting an exercise program focused on weight loss. They provide useful references that support specific approaches to achieve realistic expectations, and they review and compare various strategies.

I’m sure by March it will again be easier to find a locker at my gym. And I hope by then that my new workout plan will be more scientifically based, as well as a bit more effective. Even data-based hope springs eternal.

Judging by the crowd and the difficulty in finding a locker at my gym on January 1, a lot of people are serious about their 2016 New Year’s resolution to exercise and lose weight. But as most of us have experienced personally and professionally, embarking on a well-intended effort to exercise in the hope of losing weight more often results in frustration than a trip to the store to buy smaller-sized clothes.

The frequent answer to the question “What did the doctor say at your visit?” provides a partial explanation of this phenomenon: “Nothing, just that I should exercise and lose weight” is the usual hackneyed response. Nothing—as in nothing unexpected, nothing significant, and nothing specific was said. It is with this lack of specific advice that I feel many of us let our patients down.

We admonish patients to eat fewer calories, avoid the evil carbs, walk 10,000 steps, ride a bike, use the elliptical, or swim three times a week. There is a concrete but broad nature to these suggestions, but there is also a familiarity and a lack of specificity that leaves patients feeling that there is no science behind them. And the truth is that many of us are not comfortable enough with current data from our exercise physiology colleagues to have a detailed discussion with our patients that pairs their specific goals with an exercise regimen and diet most likely to be beneficial. We may fear sounding like the morning talk show doctors, offering sound bites instead of engaging in an evidence-based dialogue with our patients.

Many of our patients cannot afford a personal trainer to guide and cajole them through a successful regimen—assuming that they, or we, can separate myth and fact and choose an appropriate trainer. We should try to be their guide and sounding board as well as coach and cheerleader.

In this issue of the Journal, John and Christopher Higgins present a primer on the background information to use when talking with our patients about starting an exercise program focused on weight loss. They provide useful references that support specific approaches to achieve realistic expectations, and they review and compare various strategies.

I’m sure by March it will again be easier to find a locker at my gym. And I hope by then that my new workout plan will be more scientifically based, as well as a bit more effective. Even data-based hope springs eternal.

We are all exposed to initiatives from multiple stakeholders telling us to order fewer tests. Many of these efforts to control costs and improve efficiency and quality of care are directed at populations of patients and are broad concepts: provide screening only to those most likely to benefit (eg, don’t screen for prostate cancer in men with a lifespan < 10 years); avoid procedures that provided limited benefit in controlled trials (eg, limit routine arthroscopic treatment of knee osteoarthritis); and avoid reflexive practices unlikely to improve patient outcomes (eg, eliminate routine preoperative testing before elective procedures in otherwise healthy patients).

Whether system-based changes will be implemented and have an impact remains to be determined. But I sense that with all the attention being focused on population management and healthcare practices, including an emphasis on documenting and coding our encounters with patients, whether substantive or simply digital housekeeping, we are increasingly distracted from the patient in front of us and are spending less time reviewing the principles underlying the diagnoses we make and the tests we order—just as we are taking less time to perform relevant physical examinations.¹ The latter may mostly relate to time pressures. The former, I believe, is a product of both time pressures and a false sense of confidence in our knowledge of seemingly commonplace laboratory tests.

As I lecture, work with trainees, and reflect on my own patients, I realize that we are slowly but progressively minimizing the importance of a working knowledge of the basic foundations of clinical practice—perhaps because facts can always be looked up. I am not referring to knowledge of arcane biochemical pathways, eponymous references, or the latest recommended treatment of inclusion body myositis. I am thinking instead of the value of regularly refreshing our knowledge of laboratory tests and diagnoses we frequently encounter.

Having access to multiple clinical databases literally in our pockets is likely bolstering a false sense of confidence in our knowledge. The National Library of Medicine may be only a tap on a smart phone away, but accessing it regularly is a different thing. Attending conferences and reading educational journals help to keep our broad-based knowledge of internal medicine refreshed, but time pressures may significantly limit our ability to regularly pursue these activities.

In this issue of the Journal, Drs. Moghadam-Kia et al discuss their approach to asymptomatic elevations in creatine kinase (CK). Although no longer included in the most commonly used lab panels, CK measurement is often ordered in patients taking statins, even if they have no relevant muscle-related symptoms. Thus, evaluating a patient with an asymptomatic elevated CK level is not rare. The authors delve into the clinically relevant test characteristics, and their important caveats about interpreting elevated CK levels are germane not only to the asymptomatic patient, but also to the patient being evaluated for myalgia or weakness. This latter situation is one I frequently face in both the hospital and the outpatient clinic. I am often asked to consult on patients who have incompletely defined symptoms and elevated CK.

As discussed in the article, the laboratory definition of “normal” must first be considered. Laboratory test results must always be interpreted in the clinical context. An isolated elevation in parathyroid hormone cannot be interpreted without knowing the patient’s vitamin D level. Nor can “normal” low-density lipoprotein or serum urate levels be interpreted properly without knowing if the patient is accumulating excess cholesterol or urate deposits. As we order and interpret test results, we must consider the biology of the substance being measured as well as the test characteristics; too often, we react to abnormal laboratory results with an incomplete understanding of these aspects.

Moghadam-Kia et al do not dwell on the organ involvement causing CK elevations, but specificity is another very important aspect when clinically interpreting the results of a CK test. Many patients with muscle damage or inflammation have elevations in serum aspartate aminotransferase and alanine aminotransferase levels (the ratio of elevation depends on the time course of the muscle damage and on the relative clearance rate of the two enzymes). Without knowing that the CK is elevated, one might assume that an aminotransferase elevation reflects hepatitis. I have seen several patients with elevated aminotransferases and complaints of weakness and fatigue who were subjected to liver biopsy before it was recognized that the source of the enzyme elevation (“liver function test changes”) was muscle (or hemolysis). Frequently unrecognized is that aldolase, which has a cell distribution similar to that of lactate dehydrogenase, does not have the relative specificity of localization to muscle that CK has. CK is quite useful in distinguishing myocyte from hepatocyte damage.

This paper presents a wonderful reminder of the value of updating and reviewing what we know about tests that we order, even if we feel comfortable when ordering them. Before initiating a cascade of additional tests and consultations to explore the cause of an abnormal test result, a little time spent reviewing its basic characteristics and biology may pay dividends.

As 2015 comes to a close, we at the Journal share with you our sincere wishes for personal satisfaction and a globally more peaceful 2016.

We are all exposed to initiatives from multiple stakeholders telling us to order fewer tests. Many of these efforts to control costs and improve efficiency and quality of care are directed at populations of patients and are broad concepts: provide screening only to those most likely to benefit (eg, don’t screen for prostate cancer in men with a lifespan < 10 years); avoid procedures that provided limited benefit in controlled trials (eg, limit routine arthroscopic treatment of knee osteoarthritis); and avoid reflexive practices unlikely to improve patient outcomes (eg, eliminate routine preoperative testing before elective procedures in otherwise healthy patients).

Whether system-based changes will be implemented and have an impact remains to be determined. But I sense that with all the attention being focused on population management and healthcare practices, including an emphasis on documenting and coding our encounters with patients, whether substantive or simply digital housekeeping, we are increasingly distracted from the patient in front of us and are spending less time reviewing the principles underlying the diagnoses we make and the tests we order—just as we are taking less time to perform relevant physical examinations.¹ The latter may mostly relate to time pressures. The former, I believe, is a product of both time pressures and a false sense of confidence in our knowledge of seemingly commonplace laboratory tests.

As I lecture, work with trainees, and reflect on my own patients, I realize that we are slowly but progressively minimizing the importance of a working knowledge of the basic foundations of clinical practice—perhaps because facts can always be looked up. I am not referring to knowledge of arcane biochemical pathways, eponymous references, or the latest recommended treatment of inclusion body myositis. I am thinking instead of the value of regularly refreshing our knowledge of laboratory tests and diagnoses we frequently encounter.

Having access to multiple clinical databases literally in our pockets is likely bolstering a false sense of confidence in our knowledge. The National Library of Medicine may be only a tap on a smart phone away, but accessing it regularly is a different thing. Attending conferences and reading educational journals help to keep our broad-based knowledge of internal medicine refreshed, but time pressures may significantly limit our ability to regularly pursue these activities.

In this issue of the Journal, Drs. Moghadam-Kia et al discuss their approach to asymptomatic elevations in creatine kinase (CK). Although no longer included in the most commonly used lab panels, CK measurement is often ordered in patients taking statins, even if they have no relevant muscle-related symptoms. Thus, evaluating a patient with an asymptomatic elevated CK level is not rare. The authors delve into the clinically relevant test characteristics, and their important caveats about interpreting elevated CK levels are germane not only to the asymptomatic patient, but also to the patient being evaluated for myalgia or weakness. This latter situation is one I frequently face in both the hospital and the outpatient clinic. I am often asked to consult on patients who have incompletely defined symptoms and elevated CK.

As discussed in the article, the laboratory definition of “normal” must first be considered. Laboratory test results must always be interpreted in the clinical context. An isolated elevation in parathyroid hormone cannot be interpreted without knowing the patient’s vitamin D level. Nor can “normal” low-density lipoprotein or serum urate levels be interpreted properly without knowing if the patient is accumulating excess cholesterol or urate deposits. As we order and interpret test results, we must consider the biology of the substance being measured as well as the test characteristics; too often, we react to abnormal laboratory results with an incomplete understanding of these aspects.

Moghadam-Kia et al do not dwell on the organ involvement causing CK elevations, but specificity is another very important aspect when clinically interpreting the results of a CK test. Many patients with muscle damage or inflammation have elevations in serum aspartate aminotransferase and alanine aminotransferase levels (the ratio of elevation depends on the time course of the muscle damage and on the relative clearance rate of the two enzymes). Without knowing that the CK is elevated, one might assume that an aminotransferase elevation reflects hepatitis. I have seen several patients with elevated aminotransferases and complaints of weakness and fatigue who were subjected to liver biopsy before it was recognized that the source of the enzyme elevation (“liver function test changes”) was muscle (or hemolysis). Frequently unrecognized is that aldolase, which has a cell distribution similar to that of lactate dehydrogenase, does not have the relative specificity of localization to muscle that CK has. CK is quite useful in distinguishing myocyte from hepatocyte damage.

This paper presents a wonderful reminder of the value of updating and reviewing what we know about tests that we order, even if we feel comfortable when ordering them. Before initiating a cascade of additional tests and consultations to explore the cause of an abnormal test result, a little time spent reviewing its basic characteristics and biology may pay dividends.

As 2015 comes to a close, we at the Journal share with you our sincere wishes for personal satisfaction and a globally more peaceful 2016.

We are all exposed to initiatives from multiple stakeholders telling us to order fewer tests. Many of these efforts to control costs and improve efficiency and quality of care are directed at populations of patients and are broad concepts: provide screening only to those most likely to benefit (eg, don’t screen for prostate cancer in men with a lifespan < 10 years); avoid procedures that provided limited benefit in controlled trials (eg, limit routine arthroscopic treatment of knee osteoarthritis); and avoid reflexive practices unlikely to improve patient outcomes (eg, eliminate routine preoperative testing before elective procedures in otherwise healthy patients).

Whether system-based changes will be implemented and have an impact remains to be determined. But I sense that with all the attention being focused on population management and healthcare practices, including an emphasis on documenting and coding our encounters with patients, whether substantive or simply digital housekeeping, we are increasingly distracted from the patient in front of us and are spending less time reviewing the principles underlying the diagnoses we make and the tests we order—just as we are taking less time to perform relevant physical examinations.¹ The latter may mostly relate to time pressures. The former, I believe, is a product of both time pressures and a false sense of confidence in our knowledge of seemingly commonplace laboratory tests.

As I lecture, work with trainees, and reflect on my own patients, I realize that we are slowly but progressively minimizing the importance of a working knowledge of the basic foundations of clinical practice—perhaps because facts can always be looked up. I am not referring to knowledge of arcane biochemical pathways, eponymous references, or the latest recommended treatment of inclusion body myositis. I am thinking instead of the value of regularly refreshing our knowledge of laboratory tests and diagnoses we frequently encounter.

Having access to multiple clinical databases literally in our pockets is likely bolstering a false sense of confidence in our knowledge. The National Library of Medicine may be only a tap on a smart phone away, but accessing it regularly is a different thing. Attending conferences and reading educational journals help to keep our broad-based knowledge of internal medicine refreshed, but time pressures may significantly limit our ability to regularly pursue these activities.

In this issue of the Journal, Drs. Moghadam-Kia et al discuss their approach to asymptomatic elevations in creatine kinase (CK). Although no longer included in the most commonly used lab panels, CK measurement is often ordered in patients taking statins, even if they have no relevant muscle-related symptoms. Thus, evaluating a patient with an asymptomatic elevated CK level is not rare. The authors delve into the clinically relevant test characteristics, and their important caveats about interpreting elevated CK levels are germane not only to the asymptomatic patient, but also to the patient being evaluated for myalgia or weakness. This latter situation is one I frequently face in both the hospital and the outpatient clinic. I am often asked to consult on patients who have incompletely defined symptoms and elevated CK.

As discussed in the article, the laboratory definition of “normal” must first be considered. Laboratory test results must always be interpreted in the clinical context. An isolated elevation in parathyroid hormone cannot be interpreted without knowing the patient’s vitamin D level. Nor can “normal” low-density lipoprotein or serum urate levels be interpreted properly without knowing if the patient is accumulating excess cholesterol or urate deposits. As we order and interpret test results, we must consider the biology of the substance being measured as well as the test characteristics; too often, we react to abnormal laboratory results with an incomplete understanding of these aspects.

Moghadam-Kia et al do not dwell on the organ involvement causing CK elevations, but specificity is another very important aspect when clinically interpreting the results of a CK test. Many patients with muscle damage or inflammation have elevations in serum aspartate aminotransferase and alanine aminotransferase levels (the ratio of elevation depends on the time course of the muscle damage and on the relative clearance rate of the two enzymes). Without knowing that the CK is elevated, one might assume that an aminotransferase elevation reflects hepatitis. I have seen several patients with elevated aminotransferases and complaints of weakness and fatigue who were subjected to liver biopsy before it was recognized that the source of the enzyme elevation (“liver function test changes”) was muscle (or hemolysis). Frequently unrecognized is that aldolase, which has a cell distribution similar to that of lactate dehydrogenase, does not have the relative specificity of localization to muscle that CK has. CK is quite useful in distinguishing myocyte from hepatocyte damage.

This paper presents a wonderful reminder of the value of updating and reviewing what we know about tests that we order, even if we feel comfortable when ordering them. Before initiating a cascade of additional tests and consultations to explore the cause of an abnormal test result, a little time spent reviewing its basic characteristics and biology may pay dividends.

As 2015 comes to a close, we at the Journal share with you our sincere wishes for personal satisfaction and a globally more peaceful 2016.

In his physician-coming-of-age novel House of God, published in 1978, Dr. Steven Bergman (aka Sam Shem) presented rules for an intern’s survival devised by the senior resident, the Fat Man. Rule X was that there is no fever if you don’t check the patient’s temperature, implying that if the physician is unaware of an elevated temperature, no “fever workup” is warranted. A fever workup back then was not just a few keystrokes to order a chest x-ray, complete blood cell count, and blood cultures. The intern had to go to the bedside, awaken and examine the patient, draw the blood, perhaps transport the blood samples to the lab, do a urinalysis, and take the patient to the radiology department to get the chest x-ray. There was often little thought to the intern’s action; a fever in the hospital automatically meant there needed to be a fever workup.

A covering senior resident might have gotten the same notification of a fever, quickly reviewed the chart, gone to the bedside, and assessed whether a bacterial infection was likely enough to warrant the time and annoyance of a full fever workup. As supervising faculty, I will accept that assessment from a senior resident in June more willingly than from an intern in July. Tests and physical findings must be evaluated in context, taking into consideration the patient as well as the skill and experience of the physician.

So how should we react to guidelines that seem to be based on the premise that a positive finding will result in reflexive ordering of additional tests or initiating a therapeutic intervention, and thus should be avoided by all of us—young intern and senior cardiologist alike?

In this issue of the Journal, Dr. Aldo Schenone et al discuss the management of the asymptomatic patient who has carotid artery stenosis. They put into perspective the risks and benefits of medical or surgical intervention as initially defined by several landmark trials, noting how those conclusions should now be modified by knowledge of the efficacy of current medical therapy.

The US Preventive Services Task Force (USPSTF)¹ has recommended against screening for asymptomatic carotid artery stenosis in the general population, noting the limited sensitivity (71%) and specificity (98%) of auscultation to diagnose significant stenosis and lumping it with other ineffective screening tests. In other words, we should not examine asymptomatic patients for carotid bruits, just as we should not look for the fever because finding it could lead to additional testing and potentially unnecessary therapy.

But there are broader implications when a bruit is discovered, beyond simply trodding the algorithmic path toward stenting or endarterectomy. A bruit can suggest occult atherosclerotic disease that warrants medical attention, even if traditional risk factors for atherosclerosis are not prominent. Its discovery can be a wake-up call to the patient (and physician) that the hackneyed admonitions to eat healthy, lose weight, and exercise are actually relevant. Its discovery may lead to medical intervention with a potent statin or with a more aggressive target for blood pressure control. It may color the interpretation of the patient’s described vague arm tingling when bowling.

I may well be misleading myself, but I am more comfortable in dealing with whatever oddities I discover on a physical examination than not doing the examination at all. I’d rather know about the bruit (or the fever) and then think about our options. The stethoscope indeed has limited test reliability, but the real action takes place between its earpieces; the bruit is merely the catalyst for thought. There must be a guideline somewhere that says that a thoughtful, informed, commonsense evaluation is a useful contributor to patient care.

In his physician-coming-of-age novel House of God, published in 1978, Dr. Steven Bergman (aka Sam Shem) presented rules for an intern’s survival devised by the senior resident, the Fat Man. Rule X was that there is no fever if you don’t check the patient’s temperature, implying that if the physician is unaware of an elevated temperature, no “fever workup” is warranted. A fever workup back then was not just a few keystrokes to order a chest x-ray, complete blood cell count, and blood cultures. The intern had to go to the bedside, awaken and examine the patient, draw the blood, perhaps transport the blood samples to the lab, do a urinalysis, and take the patient to the radiology department to get the chest x-ray. There was often little thought to the intern’s action; a fever in the hospital automatically meant there needed to be a fever workup.

A covering senior resident might have gotten the same notification of a fever, quickly reviewed the chart, gone to the bedside, and assessed whether a bacterial infection was likely enough to warrant the time and annoyance of a full fever workup. As supervising faculty, I will accept that assessment from a senior resident in June more willingly than from an intern in July. Tests and physical findings must be evaluated in context, taking into consideration the patient as well as the skill and experience of the physician.

So how should we react to guidelines that seem to be based on the premise that a positive finding will result in reflexive ordering of additional tests or initiating a therapeutic intervention, and thus should be avoided by all of us—young intern and senior cardiologist alike?

In this issue of the Journal, Dr. Aldo Schenone et al discuss the management of the asymptomatic patient who has carotid artery stenosis. They put into perspective the risks and benefits of medical or surgical intervention as initially defined by several landmark trials, noting how those conclusions should now be modified by knowledge of the efficacy of current medical therapy.

The US Preventive Services Task Force (USPSTF)¹ has recommended against screening for asymptomatic carotid artery stenosis in the general population, noting the limited sensitivity (71%) and specificity (98%) of auscultation to diagnose significant stenosis and lumping it with other ineffective screening tests. In other words, we should not examine asymptomatic patients for carotid bruits, just as we should not look for the fever because finding it could lead to additional testing and potentially unnecessary therapy.

But there are broader implications when a bruit is discovered, beyond simply trodding the algorithmic path toward stenting or endarterectomy. A bruit can suggest occult atherosclerotic disease that warrants medical attention, even if traditional risk factors for atherosclerosis are not prominent. Its discovery can be a wake-up call to the patient (and physician) that the hackneyed admonitions to eat healthy, lose weight, and exercise are actually relevant. Its discovery may lead to medical intervention with a potent statin or with a more aggressive target for blood pressure control. It may color the interpretation of the patient’s described vague arm tingling when bowling.

I may well be misleading myself, but I am more comfortable in dealing with whatever oddities I discover on a physical examination than not doing the examination at all. I’d rather know about the bruit (or the fever) and then think about our options. The stethoscope indeed has limited test reliability, but the real action takes place between its earpieces; the bruit is merely the catalyst for thought. There must be a guideline somewhere that says that a thoughtful, informed, commonsense evaluation is a useful contributor to patient care.

In his physician-coming-of-age novel House of God, published in 1978, Dr. Steven Bergman (aka Sam Shem) presented rules for an intern’s survival devised by the senior resident, the Fat Man. Rule X was that there is no fever if you don’t check the patient’s temperature, implying that if the physician is unaware of an elevated temperature, no “fever workup” is warranted. A fever workup back then was not just a few keystrokes to order a chest x-ray, complete blood cell count, and blood cultures. The intern had to go to the bedside, awaken and examine the patient, draw the blood, perhaps transport the blood samples to the lab, do a urinalysis, and take the patient to the radiology department to get the chest x-ray. There was often little thought to the intern’s action; a fever in the hospital automatically meant there needed to be a fever workup.

A covering senior resident might have gotten the same notification of a fever, quickly reviewed the chart, gone to the bedside, and assessed whether a bacterial infection was likely enough to warrant the time and annoyance of a full fever workup. As supervising faculty, I will accept that assessment from a senior resident in June more willingly than from an intern in July. Tests and physical findings must be evaluated in context, taking into consideration the patient as well as the skill and experience of the physician.

So how should we react to guidelines that seem to be based on the premise that a positive finding will result in reflexive ordering of additional tests or initiating a therapeutic intervention, and thus should be avoided by all of us—young intern and senior cardiologist alike?

In this issue of the Journal, Dr. Aldo Schenone et al discuss the management of the asymptomatic patient who has carotid artery stenosis. They put into perspective the risks and benefits of medical or surgical intervention as initially defined by several landmark trials, noting how those conclusions should now be modified by knowledge of the efficacy of current medical therapy.

The US Preventive Services Task Force (USPSTF)¹ has recommended against screening for asymptomatic carotid artery stenosis in the general population, noting the limited sensitivity (71%) and specificity (98%) of auscultation to diagnose significant stenosis and lumping it with other ineffective screening tests. In other words, we should not examine asymptomatic patients for carotid bruits, just as we should not look for the fever because finding it could lead to additional testing and potentially unnecessary therapy.

But there are broader implications when a bruit is discovered, beyond simply trodding the algorithmic path toward stenting or endarterectomy. A bruit can suggest occult atherosclerotic disease that warrants medical attention, even if traditional risk factors for atherosclerosis are not prominent. Its discovery can be a wake-up call to the patient (and physician) that the hackneyed admonitions to eat healthy, lose weight, and exercise are actually relevant. Its discovery may lead to medical intervention with a potent statin or with a more aggressive target for blood pressure control. It may color the interpretation of the patient’s described vague arm tingling when bowling.

I may well be misleading myself, but I am more comfortable in dealing with whatever oddities I discover on a physical examination than not doing the examination at all. I’d rather know about the bruit (or the fever) and then think about our options. The stethoscope indeed has limited test reliability, but the real action takes place between its earpieces; the bruit is merely the catalyst for thought. There must be a guideline somewhere that says that a thoughtful, informed, commonsense evaluation is a useful contributor to patient care.

In Being Wrong,¹ her treatise on the psychology of human error, Kathryn Schulz quotes William James: “Our errors are surely not such awfully solemn things.”² Being wrong, she argues, is part of the human genome. Despite aphorisms such as “we learn from our mistakes,” we are far from accepting of mistakes in medical practice. Perhaps naively, I do not believe that our need to understand how clinical errors occur and how to avoid them is based on the fear of legal repercussion. And of course we do not want to harm our patients. But our relationship with medical errors is far more complex than that. We really don’t want to be wrong.

Dr. Atul Gawande³ has promoted using checklists and a structured system to limit errors of misapplication of knowledge. Diagnostic and therapeutic algorithms, once the province of trauma surgeons, are increasingly becoming part of internal medicine.

When I was a house officer we all had our “pocket brains” in our white coats—lists of disease complications, drug doses and interactions, causes of IgA deposition in the kidney, and treatment algorithms. But we believed (probably correctly) that our teachers expected us to commit all these facts to memory in our fleshy brains. The elitist and hubristic belief that this was uniformly possible has lingered in academic medicine, still permeating even the fabric of certification examinations. We learn that it is OK to be honest and say that we don’t know the answer, but we don’t like to have to say it. Physicians finish the academic game of Chutes and Ladders with a strong aversion to being wrong.

Younger doctors today seem more comfortable with not knowing so many facts and bits of medical trivia, being able to find answers instantly using their smart phones. But a challenge is knowing at a glance the context and veracity of the answers you find. And whether the knowledge comes from our anatomic, pocket, or cyber brain, the overarching challenge is to avoid Gawande’s error of misapplication.

In this issue of the Journal, Dr. Nikhil Mull and colleagues dissect a clinical case that did not proceed as expected. They discuss, in reference to the described patient, some of the published analyses of the clinical decision-making process, highlighting various ways that our reasoning can be led astray. Having just finished a stint on the inpatient consultation service, I wish I could have read the article a few weeks ago. A bit of reflection on how we reach decisions can be as powerful as knowing the source of the facts in our pocket brain.

Being wrong, as Schulz has written, is part of the human experience, but I don’t like it. Ways to limit the chances of it’s happening in the clinic are worth keeping on a personal checklist, or perhaps as an app on my smart phone.

In Being Wrong,¹ her treatise on the psychology of human error, Kathryn Schulz quotes William James: “Our errors are surely not such awfully solemn things.”² Being wrong, she argues, is part of the human genome. Despite aphorisms such as “we learn from our mistakes,” we are far from accepting of mistakes in medical practice. Perhaps naively, I do not believe that our need to understand how clinical errors occur and how to avoid them is based on the fear of legal repercussion. And of course we do not want to harm our patients. But our relationship with medical errors is far more complex than that. We really don’t want to be wrong.

Dr. Atul Gawande³ has promoted using checklists and a structured system to limit errors of misapplication of knowledge. Diagnostic and therapeutic algorithms, once the province of trauma surgeons, are increasingly becoming part of internal medicine.

When I was a house officer we all had our “pocket brains” in our white coats—lists of disease complications, drug doses and interactions, causes of IgA deposition in the kidney, and treatment algorithms. But we believed (probably correctly) that our teachers expected us to commit all these facts to memory in our fleshy brains. The elitist and hubristic belief that this was uniformly possible has lingered in academic medicine, still permeating even the fabric of certification examinations. We learn that it is OK to be honest and say that we don’t know the answer, but we don’t like to have to say it. Physicians finish the academic game of Chutes and Ladders with a strong aversion to being wrong.

Younger doctors today seem more comfortable with not knowing so many facts and bits of medical trivia, being able to find answers instantly using their smart phones. But a challenge is knowing at a glance the context and veracity of the answers you find. And whether the knowledge comes from our anatomic, pocket, or cyber brain, the overarching challenge is to avoid Gawande’s error of misapplication.

In this issue of the Journal, Dr. Nikhil Mull and colleagues dissect a clinical case that did not proceed as expected. They discuss, in reference to the described patient, some of the published analyses of the clinical decision-making process, highlighting various ways that our reasoning can be led astray. Having just finished a stint on the inpatient consultation service, I wish I could have read the article a few weeks ago. A bit of reflection on how we reach decisions can be as powerful as knowing the source of the facts in our pocket brain.

Being wrong, as Schulz has written, is part of the human experience, but I don’t like it. Ways to limit the chances of it’s happening in the clinic are worth keeping on a personal checklist, or perhaps as an app on my smart phone.

In Being Wrong,¹ her treatise on the psychology of human error, Kathryn Schulz quotes William James: “Our errors are surely not such awfully solemn things.”² Being wrong, she argues, is part of the human genome. Despite aphorisms such as “we learn from our mistakes,” we are far from accepting of mistakes in medical practice. Perhaps naively, I do not believe that our need to understand how clinical errors occur and how to avoid them is based on the fear of legal repercussion. And of course we do not want to harm our patients. But our relationship with medical errors is far more complex than that. We really don’t want to be wrong.

Dr. Atul Gawande³ has promoted using checklists and a structured system to limit errors of misapplication of knowledge. Diagnostic and therapeutic algorithms, once the province of trauma surgeons, are increasingly becoming part of internal medicine.

When I was a house officer we all had our “pocket brains” in our white coats—lists of disease complications, drug doses and interactions, causes of IgA deposition in the kidney, and treatment algorithms. But we believed (probably correctly) that our teachers expected us to commit all these facts to memory in our fleshy brains. The elitist and hubristic belief that this was uniformly possible has lingered in academic medicine, still permeating even the fabric of certification examinations. We learn that it is OK to be honest and say that we don’t know the answer, but we don’t like to have to say it. Physicians finish the academic game of Chutes and Ladders with a strong aversion to being wrong.

Younger doctors today seem more comfortable with not knowing so many facts and bits of medical trivia, being able to find answers instantly using their smart phones. But a challenge is knowing at a glance the context and veracity of the answers you find. And whether the knowledge comes from our anatomic, pocket, or cyber brain, the overarching challenge is to avoid Gawande’s error of misapplication.

In this issue of the Journal, Dr. Nikhil Mull and colleagues dissect a clinical case that did not proceed as expected. They discuss, in reference to the described patient, some of the published analyses of the clinical decision-making process, highlighting various ways that our reasoning can be led astray. Having just finished a stint on the inpatient consultation service, I wish I could have read the article a few weeks ago. A bit of reflection on how we reach decisions can be as powerful as knowing the source of the facts in our pocket brain.

Being wrong, as Schulz has written, is part of the human experience, but I don’t like it. Ways to limit the chances of it’s happening in the clinic are worth keeping on a personal checklist, or perhaps as an app on my smart phone.